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Journal of Virology, August 2007, p. 8833-8837, Vol. 81, No. 16
0022-538X/07/$08.00+0 doi:10.1128/JVI.00612-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Christine M. A. Prat,1,2
Gwendal Le Masson,3
André Garenne,3,
and
Daniel Gonzalez-Dunia1,2*,
INSERM, U563, Centre de Physiopathologie de Toulouse Purpan, Toulouse, France,1 Université Paul-Sabatier, Toulouse, France,2 INSERM, U862, and Université Bordeaux 2, Bordeaux, France3
Received 22 March 2007/ Accepted 24 May 2007
The mechanisms whereby Borna disease virus (BDV) can impair neuronal function and lead to neurobehavioral disease are not well understood. To analyze the electrophysiological properties of neurons infected with BDV, we used cultures of neurons grown on multielectrode arrays, allowing a real-time monitoring of the electrical activity across the network shaped by synaptic transmission. Although infection did not affect spontaneous neuronal activity, it selectively blocked activity-dependent enhancement of neuronal network activity, one form of synaptic plasticity thought to be important for learning and memory. These findings highlight the original mechanism of the neuronal dysfunction caused by noncytolytic infection with BDV.
Published ahead of print on 6 June 2007.
Present address: UMR1225, INRA, École Nationale Vétérinaire de Toulouse, France.
A.G. and D.G.-D. codirected this work.
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